AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 1 94-100, Copyright © 1994 by American Physiological Society
Regulation of low-amiloride-affinity sodium channels in alveolar type II cells
G. Yue, R. L. Shoemaker and S. Matalon
Department of Anesthesiology, University of Alabama, Birmingham 35233.
We determined the mechanisms by which beta-agonists increase sodium (Na+)
currents across rat alveolar type II (ATII) cells grown in primary culture.
When ATII cells were patched in the cell-attached mode using symmetrical
Na+ solutions (150 mM Na(+)-glutamate), single-channel currents were
observed for holding potentials between -80 and 30 mV (referenced to the
pipette solution) with a single-channel conductance of 27 +/- 3 pS, a mean
open time (tau 1) of 3.3 +/- 0.15 ms and an open probability (Po) of 0.36
+/- 0.06 (n = 7). Addition of 10 microM terbutaline into the bath increased
tau 1 to 6.43 +/- 0.5 ms and Po to 0.62 +/- 0.06 (n = 7) without affecting
channel conductance. Single-channel currents with a conductance of 25 +/- 2
pS were also recorded across ATII cells patched in the inside-out mode.
Addition of 250 U/ml of protein kinase A (PKA), 1 mM ATP, and 5 mM MgCl2 in
the bath solution (150 mM Na(+)-glutamate) increased the single channel tau
1 from 3.26 +/- 0.15 to 7.38 +/- 0.38 and Po from 0.41 +/- 0.06 to 0.72 +/-
0.07 (n = 6) without altering conductance. Addition of 1 microM amiloride
or ethylisopropylamiloride (EIPA) in the pipette solution (150 mM
Na(+)-glutamate) blocked single-channel activity almost completely. Ionic
substitution experiments showed the relative permeability of Na+ to K+ and
Na+ to Cl- to be 7:1 and 8:1, respectively.(ABSTRACT TRUNCATED AT 250
WORDS)
